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T J Ruigrok

Publications and source records attributed to T J Ruigrok.

At least 73 records · Page 4Linked to original sources
PubMed1990

Cerebellar nucleo-olivary projections in the rat: an anterograde tracing study with Phaseolus vulgaris-leucoagglutinin (PHA-L).

In order to evaluate the reciprocity of olivo-cerebellar and cerebello-olivary connections, a detailed description of the cerebellar nucleo-olivary projection in the rat is presented using small, iontophoretic injections of the anterograde tracer Phaseolus vulgaris-leucoagglutinin. Sparse projections were found to arise from the rostral part of the medial cerebellar nucleus toward the lateral part of the caudal medial accessory olive. Its medial parts receive a projection from the dorsolateral protuberance of the medial cerebellar nucleus. Caudal and lateral regions of the medial cerebellar nucleus project to the "beta" group and dorsomedial cell column. Heavy olivary projections to circumscribed parts of the inferior olive were found after injections in the remaining cerebellar nuclei. The medial part of the posterior interposed nucleus connects to caudolateral areas of the rostral half of the medial accessory olive, whereas lateral areas project to more rostromedial parts. The most ventromedial part of the lateral cerebellar nucleus projects to the ventrolateral outgrowth. Adjacent medial, ventral, and caudal regions connect to the ventral leaf of the principal olive. The cerebellar origin of the projection to its dorsal leaf is located in lateral, dorsal, and rostral parts of the lateral cerebellar nucleus. The dorsolateral hump projects to the dorsomedial group of the rat inferior olive. Rostromedial projections to the dorsal accessory olive originate from the lateral part of the anterior interposed nucleus, whereas its medial parts project to more lateral and caudal regions of this olivary subnucleus. The dorsal fold of the dorsal accessory olive does not receive a projection from the cerebellar nuclei but from the lateral vestibular nucleus. No cerebellar projections were found to the dorsal cap. Relatively strong ipsilateral projections, which were the mirror images of the contralateral projections, were observed in the dorsomedial group, rostral medial accessory olive, and ventral leaf of the principal olive. When both the inferior olive and the cerebellar nuclei are considered as folded but continuous sheets of grey matter, the complete nucleo-olivary projection can be described as a simple transformation.

Animals↗
PubMed1990

Mesodiencephalic and cerebellar terminals terminate upon the same dendritic spines in the glomeruli of the cat and rat inferior olive: an ultrastructural study using a combination of [3H]leucine and wheat germ agglutinin coupled horseradish peroxidase anterograde tracing.

The mesodiencephalic and cerebellar afferents in the rostral medial accessory and principal olive of the cat and rat were studied following anterograde transport of tritiated leucine combined with anterograde transport of wheat germ agglutinin coupled horseradish peroxidase in the same animals. In all studied areas at least one-third of the labelled glomeruli appeared to contain both mesodiencephalic and cerebellar terminals. In many of these cases it was found that the terminals from both afferent systems contacted the same dendritic spines. Therefore, these olivary spines may be, as will be discussed, well suited for being involved in a timing process.

Animals↗
PubMed1990

Protective effect of danshen during myocardial ischemia and reperfusion: an isolated rat heart study.

The effect of Danshen (Radix salviae miltiorrhizae) on mechanical activity and coronary flow rate of isolated rat hearts was examined to assess the ability of Danshen to protect the myocardium against the effects of ischemia and reperfusion. After 20 min of control perfusion, in the presence or absence of Danshen, the hearts were made totally ischemic for 30 min and then reperfused for 30 min. Danshen had a negative inotropic effect and caused an increase of coronary flow rate. During post-ischemic reperfusion recovery of left ventricular developed pressure in the Danshen-treated hearts was significantly better and contracture was significantly less than in the untreated hearts. The results indicate that Danshen protects the heart against some of the deleterious effects of ischemia and reperfusion.

Angina Pectoris↗
PubMed1990

Effect of pretreatment with anipamil on a submaximal calcium paradox in the isolated rat heart.

Successive perfusion of a heart with a Ca(2+)-free and Ca(2+)-containing solution results in irreversible myocardial cell damage: the calcium paradox. Experiments were undertaken to assess whether pretreatment of rats with the new calcium antagonist anipamil (5 mg/kg body weight, twice daily for 5 days) protects the isolated heart against a submaximal calcium paradox. A submaximal calcium paradox was induced by successive perfusion with a Ca(2+)-free solution and a solution containing 0.1 mM Ca2+. Hearts from rats pre-treated with anipamil did not show a negative inotropic effect during control perfusion. During reperfusion in the presence of 0.1 Ca2+, after 10 minutes of Ca(2+)-free perfusion, creatine kinase release in hearts from treated rats was significantly less than in hearts from untreated rats (p less than 0.001). It is suggested that anipamil makes the sarcolemma less sensitive to conformational changes upon Ca2+ repletion.

Animals↗
PubMed1990

Hypertrophy of inferior olivary neurons: a degenerative, regenerative or plasticity phenomenon.

After contralateral hemi-cerebellectomy, neurons in the cat inferior olive may either degenerate, appear unchanged (affected) or become hypertrophic. Morphological and physiological aspects of the latter two cell types are studied by means of intracellular recording and injection techniques and compared to normal olivary neurons. It is demonstrated that affected and hypertrophic olivary neurons can be activated by mesodiencephalic stimulation. Affected olivary neurons are morphologically very similar to normal cells. However, they may respond with long latency action potentials only to mesodiencephalic stimulation. Hypertrophic olivary neurons have an enlarged dendritic tree and soma. The soma and proximal dendrites are studded with spine-like processes. Their reaction to mesodiencephalic stimulation is very diverse and may consist of short and/or long latency action potentials that may or may not trigger dendritic spikes. It is argued that olivary hypertrophy does not present either a degenerative or regenerative state, but that both hypertrophic as well as affected olivary neurons can survive axotomy due to a strong and continuous electrotonic coupling, made possible by destruction of the GABAergic cerebellar afferents.

Animals↗
PubMed1990

Ultrastructural study of the cat hypertrophic inferior olive following anterograde tracing, immunocytochemistry, and intracellular labeling.

Contralateral cerebellectomy can induce hypertrophy of olivary neurons in cat. In the present study we examined the ultrastructure of the cat hypertrophic inferior olive following GABA-, dopamine- and serotonin-immunocytochemistry, anterograde tracing from the mesodiencephalic junction, and intracellular labeling with HRP. Compared to normal olivary neurons the hypertrophic cells showed larger cell bodies, more and longer somatic spines which were linked by gap junctions, and longer distal dendrites with relatively few spines. The hypertrophic olivary neurons received less GABAergic boutons on their dendrites but an equal percentage was apposed to their somata as compared to normal cells. Relatively many mesodiencephalic terminals, a similar serotoninergic, and a slightly increased dopaminergic input were found. The axon of one intracellularly labeled hypertrophic cell gave off recurrent collaterals bearing varicosities filled with vesicles. These results indicated that 1) hypertrophic olivary cells are affected by trophic factors not only at the cell body but also at the level of the somatic spines, dendrites, and axon, 2) the ratio of excitatory to inhibitory terminals is increased in the hypertrophic neuropil, whereas the monoaminergic input remains stationary, and 3) the electronic coupling between hypertrophic olivary neurons has shifted from a dendritic to a more somatic location due to a relatively high number of gap junctions between the somatic spines.

Animals↗
PubMed1989

Ultrastructural study of the GABAergic, cerebellar, and mesodiencephalic innervation of the cat medial accessory olive: anterograde tracing combined with immunocytochemistry.

The rostral medial accessory olive (MAO) of the cat was studied by using an ultrastructural technique combining wheat germ agglutinin-coupled horseradish peroxidase (WGA-HRP) anterograde tracing and postembedding GABA immunocytochemistry. One group of cats received a WGA-HRP injection in the posterior interposed nucleus of the cerebellum and another group received an injection in the nucleus of Darkschewitsch. Based on differences in their morphology three types of GABAergic and three types of nonGABAergic terminals were observed. One type of GABAergic terminal was often GABA/WGA-HRP double-labeled in the cerebellar experiments, and one type of nonGABAergic terminal was often WGA-HRP-labeled in the mesodiencephalic experiments. Following injections of WGA-HRP in the cerebellar nuclei virtually all WGA-HRP-labeled terminals were GABA positive. Quantification of these GABA/WGA-HRP-double-labeled terminals showed that 1) 30% of the GABAergic terminals randomly selected from the entire neuropil were double-labeled, 2) 13% of the GABAergic terminals adjacent to perikarya were double-labeled, and 3) 34% of the GABAergic terminals strategically located next to both of the dendritic elements linked by a gap junction were double-labeled. Statistical analysis of the above data showed that significantly fewer GABAergic terminals adjacent to perikarya were double-labeled (P less than .001) than would be expected from the double-labeled proportion of the randomly selected GABAergic terminals. Following injection of WGA-HRP in the nucleus of Darkschewitsch, all WGA-HRP-labeled terminals were GABA-negative. Quantification of these terminals showed that 1) 26% of the randomly selected nonGABAergic terminals were WGA-HRP labeled, 2) 20% of the nonGABAergic terminals adjacent to perikarya were WGA-HRP labeled, and 3) 23% of the nonGABAergic terminals strategically located next to a gap junction were WGA-HRP labeled. No significant differences were found among these populations. Quantification of terminals of both groups of experiments mentioned above showed that GABAergic terminals composed 1) 38% of the randomly selected terminals, 2) 64% of the terminals apposed to perikarya, and 3) 53% of the terminals strategically located next to gap junctions. Statistical analysis of the above data showed that significantly more GABAergic terminals were located adjacent to perikarya (P less than .001) and strategically next to a gap junction (P less than .05) than would be expected from the random GABAergic innervation. The above findings of the GABAergic, cerebellar, and mesodiencephalic input are discussed with regard to their functional role in the neuronal circuitry of the ros

Afferent Pathways↗
PubMed1989

Intracellular magnesium during myocardial ischemia and reperfusion: possible consequences for postischemic recovery.

Magnesium (Mg2+) is an important regulator of cell energy metabolism, since only MgATP can serve as a substrate for ATP utilizing processes. We used 31P NMR spectroscopy to determine the complexation of ATP with Mg2+ and intracellular free Mg2+ (Mgf) in isolated rat hearts during control perfusion, ischemia and reperfusion. Atomic absorption spectrophotometry was used to determine preischemic and postischemic tissue Mg2+ and release of Mg2+ into the coronary effluent during reperfusion. Mgf increased from 0.60 mmol/l during control perfusion to greater than 6.5 mmol/l after 15 min of ischemia, while we estimated that at that time 6.7 mmol/l Mg2+ had been liberated from ATP. Less than 2% of cellular Mg2+ was released to the effluent during reperfusion after 30 min of ischemia. From spectra obtained during reperfusion the fraction of ATP that was bound to Mg2+ was calculated to be approximately 96% (compared to 94% during control perfusion), indicating that intracellular Mg2+ did not limit the metabolic use of the newly produced ATP. Mgf remained elevated during reperfusion (0.85 mmol/l). We conclude that intracellular Mg2+ deficiency due to leakage of Mg2+ to the extracellular space does not play a role in the poor postischemic recovery in this isolated rat heart model. Nevertheless, high Mg2+ prior to ischemia or during reperfusion may well be protective, due to interactions of Mg2+ with the sarcolemma or intracellular sites, affecting Ca2+,K+ and Na+ distribution and fluxes.

Adenosine Triphosphate↗
PubMed1989

Low Ca2+ reperfusion and enhanced susceptibility of the postischemic heart to the calcium paradox.

This study was designed to define the effect of postischemic low Ca2+ perfusion on recovery of high-energy phosphates, intracellular pH, and contractile function in isolated rat hearts. Phosphorus-31 nuclear magnetic resonance spectroscopy was used to follow creatine phosphate, adenosine triphosphate, intracellular inorganic phosphate, and intracellular pH during control perfusion (15 minutes), total ischemia (30 minutes), and reperfusion (30 minutes). In Group I the perfusate [Ca2+] was 1.3 mmol/l throughout the experiment, whereas in Group II the perfusate [Ca2+] was reduced to 0.05 mmol/l during the first 10 minutes of reperfusion. Hearts from Group III were not made ischemic but were subjected to 10 minutes of low Ca2+ perfusion followed by 20 minutes of normal Ca2+ perfusion. During low Ca2+ reperfusion (Group II) recovery of high-energy phosphates and pH was significantly better than in controls (Group I). However, after reexposure to normal Ca2+, metabolic recovery was largely abolished, coronary flow was suddenly impaired, and contracture developed without any rhythmic contractions. These observations indicated the occurrence of a calcium paradox rather than postponed ischemia-reperfusion damage. On the other hand, normoxic hearts (Group III) tolerated temporary perfusion with 0.05 mmol/l Ca2+ very well with respect to left ventricular developed pressure, coronary flow, and metabolic parameters. In conclusion, postischemic low Ca2+ (0.05 mmol/l) perfusion may reduce reperfusion damage, but at the same time ischemia appears to enhance the susceptibility of the heart to the calcium paradox.

Adenosine Triphosphate↗
PubMed1988

A new combination of WGA-HRP anterograde tracing and GABA immunocytochemistry applied to afferents of the cat inferior olive at the ultrastructural level.

In order to identify cerebellar terminals in the cat inferior olive which contain gamma-aminobutyric acid (GABA), a technique was developed combining anterograde transport of wheatgerm agglutinine-conjugated horseradish peroxidase (WGA-HRP) with gold-immunocytochemistry. With this technique both the HRP reaction product and the immunogold labelling can be visualized in a single ultrathin section. Our results suggest that most, if not all of the WGA-HRP-labelled cerebellar terminals in the rostral medial accessory olive (MAO) and the rostral principal olive (PO) are GABAergic. In an additional experiment the GABAergic innervation of the rostral MAO was studied in combination with WGA-HRP anterograde tracing from the rostral mesencephalon. In this case the WGA-HRP-labelled terminals were never found to be GABA-positive.

Animals↗
PubMed1988

Phospholipid reorganization and bilayer destabilization during myocardial ischemia and reperfusion: a hypothesis.

The ultrastructure of myocardial tissue was studied during ischemia and reperfusion and during reperfusion with a calcium-containing solution after a short period of calcium-free perfusion (calcium paradox). After ischemia an aggregation of the sarcolemmal intramembranous particles was observed. Subsequent reperfusion resulted in further aggregation of the intramembranous particles and disruption of the sarcolemma, which was attended with the formation and extrusion of multilamellar, lipidic structures. Similar ultrastructural changes of the sarcolemma were observed during the calcium paradox. Our hypothesis is that these changes are a result of lateral phase separation of the membrane phospholipids and destabilization of the lipid bilayer. This reorganization of phospholipids may be induced by a decrease of the intracellular pH during ischemia, and an increase of the intracellular calcium content during reperfusion after ischemia and during calcium repletion after calcium-free perfusion. These ultrastructural changes of the sarcolemma are, in our view, a consequence of the physiochemical behaviour of the sarcolemmal phospholipids.

Animals↗
PubMed1988

Protective effect of pretreatment with the calcium antagonist anipamil on the ischemic-reperfused rat myocardium: a phosphorus-31 nuclear magnetic resonance study.

To assess whether the prophylactic administration of anipamil, a new calcium antagonist, protects the heart against the effects of ischemia and reperfusion, rats were injected intraperitoneally twice daily for 5 days with 5 mg/kg body weight of this drug. The heart was then isolated and perfused by the Langendorff technique. Phosphorus-31 nuclear magnetic resonance spectroscopy was used to monitor myocardial energy metabolism and intracellular pH during control perfusion and 30 min of total ischemia (37 degrees C), followed by 30 min of reperfusion. Pretreatment with anipamil altered neither left ventricular developed pressure under normoxic conditions nor the rate and extent of depletion of adenosine triphosphate (ATP) and creatine phosphate during ischemia. Intracellular acidification, however, was attenuated. On reperfusion, hearts from anipamil-pretreated animals recovered significantly better than untreated hearts with respect to replenishment of ATP and creatine phosphate stores, restitution of low levels of intracellular inorganic phosphate and recovery of left ventricular function and coronary flow. Intracellular pH recovered rapidly to preischemic levels, whereas in untreated hearts a complex intracellular inorganic phosphate peak indicated the existence of areas of different pH within the myocardium. It is concluded that anipamil pretreatment protects the heart against some of the deleterious effects of ischemia and reperfusion. Because this protection occurred in the absence of a negative inotropic effect during normoxia, it cannot be attributed to an energy-sparing effect during ischemia. Therefore, alternative mechanisms of action are to be considered.

Animals↗
PubMed1987

Effects of the anti-cancer drug adriamycin on the energy metabolism of rat heart as measured by in vivo 31P-NMR and implications for adriamycin-induced cardiotoxicity.

In vivo 31P-NMR was used to measure the effects of the anti-tumor drug adriamycin on the energy metabolism of rat heart. The exclusive acquisition of NMR signal from cardiac muscle was assured by positioning a solenoidal radio-frequency NMR coil around the heart. Appropriate control experiments verified that 31P-NMR spectra solely originated from this organ. Acute effects occurring shortly after adriamycin administration are expressed in 31P spectra as a dose-dependent decline in the cardiac levels of phosphocreatine, after which stabilization at a new steady-state level occurs. These acute effects of a single dose are complete in 30-60 min and no significant further changes take place within 150 min after drug introduction. Longer-term effects of single high doses and of multiple lower doses were measured up to a week after the initiation of treatment. It seemed that at a total dose of 20 mg/kg, drug-induced interference with cardiac energy metabolism was more pronounced than at the same dose in the acute phase. These 31P-NMR data demonstrate that adriamycin treatment is accompanied by a decrease of the cardiac phosphocreatine/ATP ratio which might be an expression of the well-established cardiotoxicity of the drug.

Adenosine Triphosphate↗
PubMed1987

31P NMR study of intracellular pH during the calcium paradox.

Reperfusion of an isolated mammalian heart with a calcium-containing solution after a brief calcium-free perfusion results in irreversible cell damage: the calcium paradox. It has been suggested that acidification of the cytosol, as a result of hydrolysis of ATP and accumulation of calcium by mitochondria, is an important factor in the development of the calcium paradox. Phosphorus nuclear magnetic resonance (31P NMR) spectroscopy was used to investigate the course of intracellular pH during the calcium paradox in isolated rabbit heart at 37 degrees C. Intracellular pH was measured from the chemical shift of the intracellular inorganic phosphate (Pi) peak. During control perfusion and the subsequent calcium-free period intracellular pH amounted to 7.1. After induction of the calcium paradox by readmitting calcium to the perfusion fluid, intracellular pH amounted to 7.0. It is concluded that acidification of the cytosol does not play a causal role in the development of the calcium paradox.

Animals↗
PubMed1985

Dendrite distribution of identified motoneurons in the lumbar spinal cord of the turtle Pseudemys scripta elegans.

Motoneurons in the turtle lumbar spinal cord were injected with HRP by electrophoresis after being electrophysiologically identified as innervating a muscle belonging to a functional group. The distribution of dendrites was studied in transverse reconstructions of 45 motoneurons, including 11 motoneurons identified as innervating knee extensor muscles, eight motoneurons innervating hip retractor and knee flexor muscles, 14 motoneurons innervating ankle and/or toe extensors and 12 motoneurons innervating ankle and/or toe flexor muscles. The dorsal dendritic tree of motoneurons innervating distally positioned musculature (ankle and/or toe extensors and flexors) was observed to contain significantly less terminal dendritic branches compared to the dorsal dendritic trees of motoneurons innervating proximally situated (hip and knee) muscles. The distribution of dendrites within the white matter was studied by measuring the total projected length of the dendritic branches within empirically defined sectors in the transverse plane. This kind of analysis also revealed differences between the dorsal dendrites of motoneurons innervating distally and proximally positioned muscles conforming to the counts of terminal dendritic branches. It is suggested that these apparent differences in the size of the dorsal dendrite may be related to the number of synapses made by primary afferents. In the white matter, the highest dendritic density for all four groups of mononeurons was found within the central part of the lateral funiculus. However, only in the ventral funiculus could slight indications be found that the dendritic density of functionally different motoneuron groups may bear some relation to the locations of the terminations of the descending pathways known to establish monosynaptic contacts with lumbar mononeurons.

Animals↗
PubMed1985

Terminations of primary afferents on lumbar motoneurons in the turtle Pseudemys scripta elegans.

The existence of monosynaptic contacts between primary afferents and motoneurons in the lumbar spinal cord of the turtle Pseudemys scripta elegans was demonstrated by intracellular injections of horseradish peroxidase. Three afferent-motoneuron combinations were satisfactorily labeled and revealed 1, 4 and 6 contacts respectively. All contacts were made on the dorsal dendritic tree of the motoneurons. It is suggested that the contacting primary afferents are from muscle spindles.

Animals↗
PubMed1985

Ultrastructural changes of sarcolemma and mitochondria in the isolated rabbit heart during ischemia and reperfusion.

Isolated rabbit hearts were perfused by the Langendorff technique, made ischemic and subsequently reperfused. It was found that ischemia results in: (i) aggregation of the intramembranous particles in the sarcolemma and (ii) extrusion of pure lipidic multilamellar structures (liposomes) from swollen mitochondria. Subsequent reperfusion resulted in further aggregation of the sarcolemmal intramembranous particles and disruption of the sarcolemma, which was attended by the formation of liposome-like structures. Intramembrane particle aggregation is explained in terms of lateral phase separation of the membrane lipids and a reduction of repulsive forces between the membrane proteins, both induced by a decrease in pH and an increase in Ca2+ concentration intracellularly. The formation and extrusion of the multilamellar structures are discussed in terms of destabilization of the bilayer which results in a structural blebbing-off of pure lipid.

Animals↗